1. Field of the Invention
The present invention relates to a composition for preventing or treating a nerve gas-induced disease comprising a phenyl carbamate compound and a method for preventing or treating a neurological disease therewith.
2. Description of the Related Art
Organophosphorus nerve agents are the principal chemical warfare agents known to produce brain injury. They block hydrolysis of the neurotransmitter acetylcholine by inhibiting the enzyme acetylcholinesterase, resulting in greatly increased postsynaptic acetylcholine levels. This causes a spectrum of effects, including miosis, excess secretions, nausea, vomiting, and muscle fasciculations. At moderate to high doses, nerve agents also cause seizures and associated convulsions. If left untreated, seizures rapidly progress to status epilepticus (SE) and cause irreversible seizure related brain damage (SRBD).
Although there is little neuropathological data from patients who have survived nerve agent attacks, abundant evidence is available from animal models, many of which involve persistent SE. The profound brain damage produced by nerve agents was first described by Petras29; Lemercier et al30; and McLeod et al. Since then, numerous studies have greatly enhanced the understanding of neuropathology resulting from nerve agent intoxication.
Neuroprotection as a Treatment for Nerve Agent Survivors. Neuroprotection refers to the relative preservation of neuronal structure and/or function. In the case of an ongoing insult (a neurodegenerative insult) the relative preservation of neuronal integrity implies a reduction in the rate of neuronal loss over time, which can be expressed as a differential equation. It is a widely explored treatment option for many central nervous system (CNS) disorders. Neuroprotection aims to prevent or slow disease progression and secondary injuries by halting or at least slowing the loss of neurons. Neuroprotective treatments often target oxidative stress and excitotoxicity. both of which are highly associated with CNS disorders. Not only can oxidative stress and excitotoxicity trigger neuron cell death but when combined they have synergistic effects that cause even more degradation than on their own. Thus limiting excitotoxicity and oxidative stress is a very important aspect of neuroprotection.
Throughout this application, various publications and patents are referred and citations are provided in parentheses. The disclosures of these publications and patents in their entities are hereby incorporated by references into this application in order to fully describe this invention and the state of the art to which this invention pertains.